Acutely, alcohol also leads to the stimulation of eicosanoid production with an increased PGI2/TXA2 resulting in decreased vascular tone and platelet aggregabilitity. Chronic alcohol exposure, on the other hand, leads to a decrease in polyunsaturated fats, especially in the AA and DHA components of blood cells and vascular smooth muscle. This LCP decrease is likely caused by a potent stimulation of fatty acid catabolism as reflected in lipid peroxides, aldehydes and eicosanoids as well as isoprostanes. Chronic alcohol exposure also leads to a decreased eicosanoid production from platelets and smooth muscle resulting in a decreased PGI2/TXA2 ratio and increased vascular tone. The losses in membrane phospholipid LCPs, the increases in fatty acid catabolites and the alteration in eicosanoid balance may underlie, in part, the pathophysiology associated with alcoholism, including hypertension, angina, myocardial infarct and stroke.
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